Evidence map›Paper›PMID 27629507›Full record

ReviewNature reviews. Cardiology2016

Pathogenesis and management of Brugada syndrome.

Juan Sieira, Gregory Dendramis, Pedro Brugada

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Cardiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed, 1 pooled it
10.5field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

56 citing papers in PubMed, 1 synthesis or guideline pooled it, 125 citations in OpenAlex.

  1. A systematic review and meta-analysis of artificial intelligence ECGs performance in the diagnosis of Brugada Syndrome.Journal of interventional cardiac electrophysiology : an international journal of arrhythmias and pacing · 2026
    Pooled it
  2. Phase 2 Re-Entry Without IJACC. Clinical electrophysiology · 2023
    Trial
  3. Magnetic field based investigation of Brugada syndrome.European biophysics journal : EBJ · 2026
    Article
  4. Review
  5. Gene Therapy for Inherited Cardiac Arrhythmias.Journal of cardiovascular translational research · 2025
    Review
  6. Article
  7. Cardiac Channelopathies: Clinical Diagnosis and Promising Therapeutics.Journal of the American Heart Association · 2025
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Primary Electrical Heart Disease-Principles of Pathophysiology and Genetics.International journal of molecular sciences · 2024
    Review
  13. Identification of a novelFrontiers in cardiovascular medicine · 2024
    Article
  14. Article
  15. Review
  16. Article
  17. Appropriate and inappropriate therapies in remotely monitored patients with Brugada syndrome: what to expect?Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2023
    Article
  18. Review
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Juan SieiraHeart Rhythm Management Centre, UZ Brussel-VUB, Brussels, Laarbeeklaan 101, 1090 Brussels, Belgium.
Gregory DendramisHeart Rhythm Management Centre, UZ Brussel-VUB, Brussels, Laarbeeklaan 101, 1090 Brussels, Belgium.
Pedro BrugadaHeart Rhythm Management Centre, UZ Brussel-VUB, Brussels, Laarbeeklaan 101, 1090 Brussels, Belgium.
Universitair Ziekenhuis Brussel · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Brugada syndrome is an inherited disease characterized by an increased risk of sudden cardiac death owing to ventricular arrhythmias in the absence of structural heart disease. Since the first description of the syndrome >20 years ago, considerable advances have been made in our understanding of the underlying mechanisms involved and the strategies to stratify at-risk patients. The development of repolarization-depolarization abnormalities in patients with Brugada syndrome can involve genetic alterations, abnormal neural crest cell migration, improper gap junctional communication, or connexome abnormalities. A common phenotype observed on the electrocardiogram of patients with Brugada syndrome might be the result of different pathophysiological mechanisms. Furthermore, risk stratification of this patient cohort is critical, and although some risk factors for Brugada syndrome have been frequently reported, several others remain unconfirmed. Current clinical guidelines offer recommendations for patients at high risk of developing sudden cardiac death, but the management of those at low risk has not yet been defined. In this Review, we discuss the proposed mechanisms that underlie the development of Brugada syndrome and the current risk stratification and therapeutic options available for these patients.

Indexed as

Anti-Arrhythmia AgentsBrugada SyndromeCatheter AblationDeath, Sudden, CardiacDefibrillators, ImplantableElectrocardiographyElectrophysiological PhenomenaHumansQuinidineRisk AssessmentRisk FactorsAnti-Arrhythmia AgentsQuinidine

Identifiers

PMID27629507
OpenAlexW2520637003

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.